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Procaine Inhibits the Proliferation and Migration of Colon Cancer Cells Through Inactivation of the ERK/MAPK/FAK Pathways by Regulation of RhoA

Chang Li^*, Shuohui Gao^*, Xiaoping Li^†, Chang Li^‡, Lianjun Ma^§

* Department of Gastrointestinal Surgery, China–Japan Union Hospital of Jilin University, Changchun, P.R. China
† Department of Pediatrics, The First Bethune Hospital of Jilin University, Changchun, P.R. China
‡ Department of Cadre’s Ward, China–Japan Union Hospital of Jilin University, Changchun, P.R. China
§ Endoscopy Center, China–Japan Union Hospital of Jilin University, Changchun, P.R. China

Oncology Research 2020, 28(6), 675-679. https://doi.org/10.3727/096504021X16137463165406

Abstract

Colon cancer is one of the most lethal varieties of cancer. Chemotherapy remains as one of the principal treatment approaches for colon cancer. The anticancer activity of procaine (PCA), which is a local anesthetic drug, has been explored in different studies. In our study, we aimed to explore the anticancer effect of PCA on colon cancer and its underlying mechanism. The results showed that PCA significantly inhibited cell viability, increased the percentage of apoptotic cells, and decreased the expression level of RhoA in HCT116 cells in a dose-dependent manner (p < 0.05 or p < 0.01). Moreover, PCA increased the proportion of HCT116 cells in the G₁ phase as well as downregulated cyclin D1 and cyclin E expressions (p < 0.05). In addition, we found that PCA remarkably inhibited cell migration in HCT116 cells (p < 0.01). However, all these effects of PCA on cell proliferation, apoptosis, and migration were significantly reversed by PCA + pc-RhoA (p < 0.05 or p < 0.01). PCA also significantly decreased the levels of p-ERK, p-p38MAPK, and p-FAK, but PCA + pc-RhoA rescued these effects. Furthermore, the ERK inhibitor (PD098059), p38MAPK inhibitor (SB203580), and FAK inhibitor (Y15) reversed these results. These data indicate that PCA inhibited cell proliferation and migration but promoted apoptosis as well as inactivated the ERK/MAPK/FAK pathways by regulation of RhoA in HCT116 cells.

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